There is evidence from the literature that the syndrome of neuroleptic-induced tardive dyskinesia represents a defect in the balance between acetylcholine and dopamine mediated activity converging on neurons of the striatum. Treatment with deanol, a possible acetylcholine precursor, has produced variable results which need further study. Preliminary study of six patients has shown that acute drug challenges with dopamine and acetylcholine agonists and antagonists can temporarily modify the movements of tardive dyskinesia. The response to physostigmine significantly predicted the response to deanol. The results as a whole suggest the possibility that there are two pharmacologically distinct subgroups of clinical tardive dyskinesia. Patients with tardive dyskinesia will be treated on five consecutive days with a dopamine agonist (apomorphine), a dopamine antagonist (droperidol), and acetylcholine agonist (physostigmine), an acetylcholine antagonist (biperiden), and a placebo, and the effects on eye-blinking and mouth and extremity movements measured objectively. The patients are then randomly assigned in a double blind paradigm to deanol or placebo for four weeks in increasing doses until improvement occurs or side effects intervene. A crossover is instituted after four weeks. The pharmacological profile obtained initially will be correlated with the presence or absence of a deanol therapeutic response. Spectral analysis of the movements will also be used to identify drug responders. These data may make it possible to detect deanol responders prospectively, identify subgroups within the syndrome, define underlying mechanisms, and perhaps shed light on the pathophysiology of other movement disorders as well.